The dysregulated activity of effector cells of the TH1 and TH17 subsets of helper T cells results in the development of tissue inflammation and autoimmunity. Myelin-specific TH1 and TH17 cells, for example, contribute to disease pathogenesis in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). Nylander and Hafler, J. Clin. Invest (2012) 122:1180-188; and Pierson et al. Immunol. Rev. (2012) 248: 205-215. During EAE, dendritic cells (DCs) control the activation and differentiation of myelin-specific effector T cells and regulatory T cells (Treg cells). Bailey et al. Nat. Immunol. (2007) 8:172-180; and Yogev et al. Immunity (2012)37: 264-275. Moreover, DCs isolated from patients with MS generally produce large amounts of TH1- and TH17-polarizing cytokines. Comabella et al. Nat. Rev. Nephrol. (2010) 6: 499-507. DCs control several pathogenic mechanisms associated with the development of central nervous system (CNS) autoimmunity. DCs promote the entry of T cells into the CNS, the activation and differentiation of pathogenic T cells in the CNS, and the spreading of the autoimmune response to new CNS epitopes. Greter et al. Nat. Med. (2005) 11: 328-334; Bailey et al. Nat. Immunol. (2007) 8:172-180; and McMahon et al. Nat. Med. (2005) 11:335-339. Accordingly, there is a need to identify pathways that regulate DC activity during the course of autoimmunity, to identify mechanisms of disease pathogenesis and also to develop new approaches for therapeutic intervention to treat an autoimmune disease.